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Introduction
Due to its high metastasis and invasion, glioblastoma is the most common malignant tumor of the central nervous system (CNS) in adults with poor prognoses (1), and a median survival of ~10–14 months after the initial diagnosis (2). Accordingly, the recurrence of gliomas remains unavoidable. Currently, early diagnosis and a multimodal approach are the basic requirements for glioma treatments, which include surgical resection, chemotherapeutics and radiotherapy and have an extremely poor prognosis. The major challenges for glioma treatment include many barriers, such as the extent of surgical resection and resistance to radiotherapy and chemotherapy (3). Thus, it is important to explore more efficacious measures against glioma to address the aforementioned issues, and there is an urgent need to develop new compounds against glioma.
Epidermal growth factor receptor (EGFR) is a member of the HER family, which also includes HER2, HER3 and HER4, and EGFR has been identified as an oncogene in many malignant tumors (4,5). EGFR and its downstream signaling pathways are pivotal regulators of many cellular processes, including cell differentiation, metabolism, proliferation and survival, in a large variety of tumors (6–8). EGFR is also overexpressed in most gliomas (9). Therefore, therapies that target EGFR and its downstream signaling pathways may be potential treatments for glioblastoma.
Oxymatrine (OM), a natural quinolizidine alkaloid that is the principal component of the traditional Chinese herb Sophora flavescens, has been reported to produce a great diversity of pharmacological effects, such as anti-inflammatory, antiviral, immunoregulatory and anti-apoptosis effects. Originally, OM was used for the treatment of viral hepatitis (10–14). More recent in vitro studies have revealed the significant antitumor activity of OM in the cells of many human cancers, including hepatic (15), pancreatic (16,17), gastric (18) and colorectal carcinoma (19), as well as mastocarcinoma (20). However, the antitumor activity of OM in glioma cells has been rarely studied and the mechanism by which OM exerts its antitumor effect against glioma has not been reported.
In the present study, we studied the effect of OM on glioblastoma cells. We found that OM markedly suppressed the proliferation and invasion, as well as promoted the apoptosis of glioma cells. Further studies revealed that OM arrested the cell cycle at the G0/G1 phase and decreased the protein expression levels of cyclin D1...